Practical Guidelines for Diagnosing and Treating Thyroid Disease Based on the WOMED Metabolic Model of Disease Focusing on Glycolysis and Coenzyme Q10 Deficiency—A Clinical Alternative to the 2021 Retired Clinical Practice Guidelines of the Endocrine Society

Abstract

This review aims to provide a functional, metabolic view of the pathogenesis of benign thyroid disease. Here, we summarize the features of our previous publications on the “WOMED model of benign thyroid disease”. As of 2021, the current state of art indicates that the basic alteration in benign thyroid disease is a metabolic switch to glycolysis, which can be recognized using 3D-power Doppler ultrasound. A specific perfusion pattern showing enlarged vessels can be found using this technology. This switch originates from an altered function of Complex I due to acquired coenzyme Q10 deficiency, which leads to a glycolytic state of metabolism together with increased angiogenesis. Implementing a combined supplementation strategy that includes magnesium, selenium, and CoQ10, the morphological and perfusion changes of the thyroid can be reverted, i.e., the metabolic state returns to oxidative phosphorylation. Normalization of iron levels when ferritin is lower than 50 ng/mL is also imperative. We propose that a modern investigation of probable thyroid disease requires the use of 3D-power Doppler sonography to recognize the true metabolic situation of the gland. Blood levels of magnesium, selenium, CoQ10, and ferritin should be monitored. Thyroid function tests are complementary so that hypo- or hyperthyroidism can be recognized. Single TSH determinations do not reflect the glycolytic state.

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

“…The central issue is loss of mitochondrial function due to CoQ10 deficiency. In a series of publications, we have demonstrated both this pathogenetic principle as well as the treatment strategy for thyroid disease [121][122][123][124][125]. One key event related to CoQ10 deficiency is the development of hypoxia [126].…”

Coenzyme Q10 and Autoimmune Disorders: An Overview

“…Pre-clinical research and a small clinical study indicate CoQ10 supplementation may help improve cardiac performance in those with hyperthyroidism [68,71,80]. A therapeutic regime supplementing CoQ10 (60 mg/day ongoing) for the correction of CoQ10 deficiency in patients with thyroid disease has been described by Moncayo and Moncayo [81].…”

Thyroid-associated ophthalmopathy: the role of oxidative stress

“…Additionally, vitamin C and E supplementation improved clinical symptoms and clinical scores in TAO patients by reducing oxidative stress markers ( 131 ). These antioxidants inhibit TAO fibroblast proliferation, with N-acetylcysteine and melatonin selectively blocking IFN-γ release ( 132 ). They also reduce HA and IL-1β levels in orbital fibroblasts of TAO patients and normal controls ( 133 ).…”